Evidence map›Paper›PMID 10766742›Full record

ArticleGenes & development2000

The Drosophila HEM-2/NAP1 homolog KETTE controls axonal pathfinding and cytoskeletal organization.

T Hummel, K Leifker, C Klämbt

Open access · diamondAbstract read
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Article in Genes & development, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 82 citations in OpenAlex.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

T HummelInstitut für Neurobiologie, Universität Münster, D-48149 Münster, Germany.
K Leifker
C Klämbt
University of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In Drosophila, the correct formation of the segmental commissures depends on neuron-glial interactions at the midline. The VUM midline neurons extend axons along which glial cells migrate in between anterior and posterior commissures. Here, we show that the gene kette is required for the normal projection of the VUM axons and subsequently disrupts glial migration. Axonal projection defects are also found for many other moto- and interneurons. In addition, kette affects the cell morphology of mesodermal and epidermal derivatives, which show an abnormal actin cytoskeleton. The KETTE protein is homologous to the transmembrane protein HEM-2/NAP1 evolutionary conserved from worms to vertebrates. In vitro analysis has shown a specific interaction of the vertebrate HEM-2/NAP1 with the SH2-SH3 adapter protein NCK and the small GTPase RAC1, which both have been implicated in regulating cytoskeleton organization and axonal growth. Hypomorphic kette mutations lead to axonal defects similar to mutations in the Drosophila NCK homolog dreadlocks. Furthermore, we show that kette and dock mutants genetically interact. NCK is thought to interact with the small G proteins RAC1 and CDC42, which play a role in axonal growth. In line with these observations, a kette phenocopy can be obtained following directed expression of mutant DCDC42 or DRAC1 in the CNS midline. In addition, the kette mutant phenotype can be partially rescued by expression of an activated DRAC1 transgene. Our data suggest an important role of the HEM-2 protein in cytoskeletal organization during axonal pathfinding.

Indexed as

Gene Expression Regulation, DevelopmentalAdaptor Proteins, Signal TransducingAmino Acid SequenceAnimalsAxonsCell Cycle ProteinsConserved SequenceCytoskeletonDrosophilaDrosophila ProteinsEmbryo, NonmammalianEthyl MethanesulfonateInsect ProteinsMembrane ProteinsMutagenesisNerve Growth FactorsAdaptor Proteins, Signal TransducingCell Cycle Proteinsdock protein, DrosophilaDrosophila ProteinsEthyl MethanesulfonateInsect ProteinsMembrane ProteinsNap1 protein, DrosophilaNerve Growth FactorsNerve Tissue ProteinsNuclear ProteinsNucleosome Assembly Protein 1Proteins

Identifiers

PMID10766742
PMCPMC316499
OpenAlexW2149119048

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.